Peer Reviewed
New Onset of Severe Mitral Valve Regurgitation Status Post COVID-19 Recovery
Introduction. A 43-year-old man presented to his primary care physician for a routine physical examination. At this visit, the patient reported elevated blood pressure, headaches, fatigue, new onset of palpitations, and exertional dyspnea for the past 2 months, following a polymerase chain reaction-confirmed COVID-19 infection.
History. Prior to this visit, the patient had no history of cardiac diagnosis or symptoms with exertional activity. The patient endorses frequent extensive physical activity at baseline. The patient had no recent dental procedures or maxillofacial surgery.
At presentation, the patient's vitals were a heart rate of 112 beats/min, blood pressure of 150/90 mm Hg, 97% oxygen saturation level on room air, and temperature of 98.1° F.
Diagnostic testing. The patient's electrocardiogram (EKG) was indicative of sinus tachycardia. The EKG revealed a new blowing holosystolic murmur at the apex radiating to the left axilla, indicative of mitral valve regurgitation on auscultation of the anterior chest wall (Figures 1 and 2). No clinical evidence of congestive heart failure, including leg edema or pulmonary auscultation pathology, was observed. There was also no lymphadenopathy or dermatological findings.
Figure 1. Echocardiogram showing mitral valve regurgitation on color doppler prior to surgical correction.
Figure 2. Echocardiogram showing mitral valve regurgitation on pulse wave doppler prior to surgical correction.
Aerobic and anaerobic blood cultures were negative with no growth after 5 days. The comprehensive metabolic panel was grossly unremarkable. White blood cell count, hematocrit, and hemoglobin were within normal limits. The echocardiogram indicated normal left ventricular ejection fracture, with severe mitral regurgitation/insufficiency. Based on the clinical history and echocardiogram, a diagnosis of severe mitral regurgitation was made.
Differential diagnoses. After initial presentation and physical examination, the differential diagnosis included bacterial endocarditis, cardiac ischemia, calcified aortic stenosis, cardiac mass, and dilated cardiomyopathy. Endocarditis was ruled out after receiving negative blood cultures and histologic testing of the valvular specimen. Ischemia was an unlikely diagnosis due to no acute or chronic ischemic changes on electrocardiogram, as well as normal troponin I and B-type natriuretic peptide values. Aortic stenosis, cardiac mass, and dilated cardiomyopathy were not present on preoperative echocardiogram, and thus ruled out.
Treatment and management. The patient was then sent for minimally invasive mitral valve repair with primary closure of the left primary atrial appendage. The pathological specimen suggested fibroelastic deficiency of the valve with thin translucent leaflets and chordae. The Effective Regurgitant Orifice Area (EROA) was found to be 0.5 +/- 5cm2 and regurgitation volume was 93.4 mmL/beat. These both indicate severe mitral valve insufficiency, as severe mitral valve regurgitation is defined as equal to or greater than 0.4 cm2 for EROA and equal to or greater than 60.0 mmL/beat for regurgitation volume.1
Outcome and follow-up. The patient had an uneventful postoperative recovery. A repeat echocardiogram was performed postoperatively during his hospital stay and showed excellent repair with trace residual insufficiency, as well as normal mitral leaflet motion and normal left ventricular motion. Chest x-ray showed stable cardiac and mediastinal silhouette status post mitral valve repair.
Discussion. COVID-19 infection can induce a variety of clinical presentations. While the most notable is acute respiratory distress syndrome, other presentations include cytokine storm, myocarditis, hypercoagulability, and more.2 It is well known that SARS-CoV-2 depends on the angiotensin-converting enzyme 2 (ACE2) receptor for entry into cells. Recently, this receptor was shown to be present in cardiac myocytes and, more importantly for this discussion, cardiac valves.3-5 Using the ACE2 receptor for entry into the cell causes downregulation of this receptor which has been related to inflammation, proliferation, and fibrosis in cardiac valves.5,6
Additionally, patients diagnosed with COVID-19 induced myocarditis have been found to have fibrosis in the histological samples of the myocardium, though it is uncertain if this is due to the myocarditis or other chronic cardiac conditions.7 The use of ACE2 receptor entry into the cell along with the proposed cytokine storm induced by COVID-19 both result in inflammation of cardiac tissues, which is well known to result in fibrosis.8,1
Bacterial infection resulting in valvular dysfunction and failure is one of the most common causes of valve dysfunction in underdeveloped countries and to a lesser extent in developed countries. The gram-positive organisms of streptococci, staphylococci, and enterococci account for roughly 80% to 90% of infectious endocarditis.9 Risk factors in developed countries mainly include recent procedures such as dental manipulation or cardiac catheterization, or intravenous drug use.10 With infectious endocarditis, blood cultures then intravenous antibiotics are the mainstay of initial treatment. Depending on the severity of infection and damage that has occurred, surgical intervention such as valvular repair or replacement may be needed. This is contrasted with congenital and rheumatologic valvular degeneration, which is monitored until severity requires surgical intervention.
In this case, we discussed a 43-year-old man with no previous detection of cardiac disease who suddenly developed cardiac symptoms resulting in a diagnosis of severe mitral valve insufficiency months after testing positive for COVID-19. We propose that this patient's mitral valve failure and subsequent need for corrective surgery were due to complications from his infection with COVID-19. While it is possible that this patient had asymptomatic mitral valve disease prior to COVID-19 infection, the lack of prior symptoms or prior detection of cardiac disease led us to attribute the histological changes in our patient's mitral valve to be directly due to the SARS-CoV-2 infection he suffered prior to valve failure.
This finding may be an acute and/or chronic condition brought on after COVID-19 infection. Prospective studies should evaluate the outcomes of valvular dysfunction in relation to COVID-19 recovery.
AFFILIATIONS
1Touro College of Osteopathic Medicine, Middletown, NY
2Clinical Adjunct Assistant Professor of Medicine, Touro College of Osteopathic Medicine; Mid Hudson Medical Research; Horizon Family Medical Group, New Windsor, NY
CITATION
Bayly B, Hasan F, Makam S. New onset of severe mitral valve regurgitation status post COVID-19 recovery. Consultant. 2023;63(9):e4. doi:10.25270/con.2023.08.000009
Received September 19, 2022. Accepted January 26, 2023. Published online August 16, 2023.
DISCLOSURES
The authors report no relevant financial relationships.
ACKNOWLEDGEMENTS
None.
CORRESPONDENCE
Benjamin Bayly, Tuoro College of Osteopathic Medicine, 26 Wetsel Road, Troy, NY 12182 (bbayly9@yahoo.com)
- Suthahar N, Meijers WC, Silljé HH, de Boer RA. From inflammation to fibrosis—molecular and cellular mechanisms of myocardial tissue remodelling and perspectives on differential treatment opportunities. Curr Heart Fail Rep. 2017;14:235–250. doi:10.1007/ss11897/017-0343-y.
- Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395:1417–1418. doi:10.1016/S0140-6736(20)30937-5.
- Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020;181:271–280. doi:10.1016/j.cell.2020.02.052.
- Chen L, Li X, Chen M, Feng Y, Xiong C. The ACE2 expression in the human heart indicates a new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res. 2020;116(6):1097–1100. doi:10.1093/cvr/cvaa078.
- Peltonen T, Näpänkangas J, Ohtonen P, et al. (Pro)renin receptors and angiotensin converting enzyme 2/angiotensin-(1-7)/Mas receptor axis in human aortic valve stenosis. Atherosclerosis. 2011;216(1):35–43. doi:10.1016/j.atherosclerosis.2011.01.018.
- Kuba K, Imai Y, Rao S, et al. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat Med. 2005;11(8):875-879. doi:10.1038/nm1267.
- Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury: a multicentre cardiovascular pathology study. Eur Heart J. 2020;41(39):3827-3835. doi:10.1093/eurheartj/ehaa664.
- Chen, C., Zhou, Y.& Wang, D.W. SARS-CoV-2: a potential novel etiology of fulminant myocarditis. Herz. 2020;45(3):230-232. doi:10.1007/s00059-020-04909-z
- Barnett R. Infective endocarditis. Lancet. 2016;388(10050):1148. doi:10.1016/S0140-6736(16)31602-6
- Hill EE, Herijigers P, Claus P, Vanderschueren S, Herregods MC, Peetermans WE. Infective endocarditis: changing epidemiology and predictors of 6-month mortaility: a prospective cohort study. Eur Heart J. 2007;28(2):196-203. doi:10.1093/eurheartj/ehl427.